Page 313 - Avian Virology: Current Research and Future Trends

304 | Corredor and Nagy

and persistent infection have been studied in mainly mastad- Epizootiology
enoviruses. Modulation of the host’s immune response by Avian adenoviruses have a worldwide distribution in commer-
mastadenovirus E3 proteins is linked to latent and persistent cial poultry (e.g. chickens, turkey, ducks, goose, quail, ostrich,
infections. Such infections can be the result of differential expres- etc.) and wild birds. Some virus strains cause mild or no disease
sion of viral and cellular genes in a cell-type dependent manner whereas pathogenic viruses are associated with economically
(Murali et al., 2014; Ornelles et al., 2016). important diseases. These diseases include IBH, GE and HPS
As also mentioned, IFN signalling promotes the establish- caused by FAdVs, HE caused by HEV and EDS caused by EDSV.
ment of the antiviral state. However, recent studies with HAdV-5 Depending on the virus range, some of these viruses can cause
suggest the role of types I and II IFNs in suppressing the lytic different diseases in poultry species. For example, FAdV-1 causes
cycle and promoting the establishment of latency. Establish- bronchitis in quails and IBH/GE in chickens; EDSV can infect
ment of latency by IFN seems to be the result of repression of chicken, goose and duck; HEV infects turkey and chicken causing
transcription of E1A genes in a cell-type specific manner. IFNs HE and marble spleen disease (MSD), respectively; FAdV-4 can
have been found to increase the repression of the E1A genes by cause HPS in chicken, ostrich and duck (McFerran and Smyth,
tumour suppressors pRb and p107, probably by competing with 2000; Changjing et al., 2016). Different viral agents can cause
GABP α/β for the E1A enhancer, during the early phase of infec- similar clinical signs seen in chickens. For example, GoAdV and a
tion. Removal of IFN leads to the expression of E1A genes and member of TAdV-D are associated with clinical signs of HPS with
reactivation of the lytic cycle (Zheng et al., 2016). The role of IFN increased mortality in goslings and turkeys, respectively (Ivanics
on the establishment of persistent infections and latency by avian et al., 2010; Kleine et al., 2017).
adenoviruses is unknown. The epizootiology of diseases caused by these viruses and
Reactivation of avian adenoviruses from latency is believed their negative impacts in the poultry industry has been reported
to occur after maternal antibody wanes or under stress condi- in many countries including China, Japan, Pakistan, India, Iran,
tions, such as the onset of egg production (Girshick et al., 1980; Korea, Poland, Germany, Spain, Australia and the Americas
Philippe et al., 2007). Persistent virus shedding through the faeces (Hess et al., 1999; Ono et al., 2003; Gomis et al., 2006; Ojkic
can occur after several weeks of infection or throughout the birds’ et al., 2008a; Choi et al., 2012; Dar et al., 2012; Asthana et
life, even in the presence of neutralizing antibodies (McFerran al., 2013; Changjing et al., 2016; Gaweł et al., 2016; Li et al.,
and Smyth, 2000). Persistent infections have been observed with 2016; Singh et al., 2016; Zhang et al., 2016; Kleine et al., 2017;
avirulent strains used for vaccination, such as the Virginia aviru- Morshed et al., 2017; Oliver-Ferrando et al., 2017). For exam-
lent strain (VAS) of HEV. It is suggested that persistent infection ple, epizootiological studies conducted in broiler hatcheries in
with VAS modulates the immune response to HEV and provide Ontario, Canada, between 2007 and 2009, showed an annual
more than 20 weeks protection after vaccination (Beach et al., loss of 105,000 broilers ($300,000 CAD) due to IBH outbreaks
2009b). (Dar et al., 2012).
Virus-induced immunosuppression as a consequence of lym- Most epizootiological studies have confirmed FAdV-4 as the
phocytic depletion in the bursa of Fabricius, thymus and spleen is causative agent for HPS (Naeem et al., 1995; Asthana et al., 2013;
associated with the decline of T- and B-cell populations due to the Schachner et al., 2018), though studies conducted in India and
predilection of virulent FAdVs (serotypes 1, 4 and-8) and HEV to China suggest its association with other serotypes (e.g. FAdV-12),
lymphoid tissues (Saifuddin and Wilks, 1992; Naeem et al., 1995; either alone or in combination with FAdV-4 (Rahul et al., 2005).
Singh et al., 2006; Asthana et al., 2013). IBH has been associated with nearly all FAdVs serotypes, mainly
Infections with HEV causes severe splenic lesions accompa- FAdV-2, FAdV-8a, FAdV-8b and FAdV-11 (Schachner et al.,
nied by lymphoid necrosis and a massive disintegration of the 2018). IBH and HPS have being regarded as secondary diseases
white pulp. These T- and B-cell disbalances result in significant requiring concurrent infection with immunosuppressive agents,
decreases in the production of IgM antibodies (Saifuddin such as chicken anaemia virus (CAV) or infectious bursal dis-
and Wilks, 1992; Suresh and Sharma, 1995; Singh et al., 2006; ease virus (IBDV) (Hess, 2013). Some epizootiological studies
Schonewille et al., 2008) and lead to secondary infections and conducted in different countries such Korea, China and Chile
disease development. As mentioned above, increases in CD8+ have suggest the association between CAV and IBH/HPS (Toro
cells relative to CD4+ cells as a consequence of HEV infection et al., 1999; Choi et al., 2012; Changjing et al., 2016). However,
are thought to play an important role in HE (Suresh and Sharma, a great number of epizootiological studies conducted in many
1995). Infection with HEV has been found to predispose birds to countries in the last 15 years have increased the awareness of
enteropathogenic E. coli infection, either naturally or experimen- FAdVs as primary agents causing outbreaks of IBH in the absence
tally, and clostridial dermatitis. HEV infection is also associated of immunosuppressive agents (Reece et al., 1986; Saifuddin and
with poor antibody response to vaccines, such as ones used Wilks, 1990a; Gomis et al., 2006; Steer et al., 2011; Schachner et
against Newcastle disease (Dhama et al., 2017). The negative al., 2018).
effects of FAdV infections on the humoral immune response, as Increasing numbers of IBH outbreaks in different geographic
determined by antibodies to sheep red blood cells and Brucella locations for the last two decades suggest worldwide spread of the
abortus, have also been reported for pathogenic FAdVs (Saifuddin disease. IBH principally affects 3–5-week-old broilers and spo-
and Wilks, 1992; Singh et al., 2006). radically layers and broiler breeders. Mortality peaks within 3–4